Evidence map›Paper›PMID 19506027›Full record

ArticleNucleic acids research2009

A physical and functional link between splicing factors promotes pre-mRNA 3' end processing.

Stefania Millevoi, Adrien Decorsière, Clarisse Loulergue, Jason Iacovoni, Sandra Bernat, Michael Antoniou, Stéphan Vagner

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 67 citations in OpenAlex.

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  7. RNA in cancer.Nature reviews. Cancer · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Stefania MillevoiINSERM, U563, Toulouse, Université de Toulouse, UPS, Centre de Physiopathologie de Toulouse Purpan, Toulouse, F-31300, France. stefania.millevoi@inserm.fr
Adrien Decorsière
Clarisse Loulergue
Jason Iacovoni
Sandra Bernat
Michael Antoniou
Stéphan Vagner
King's College London · GBUniversité Toulouse III - Paul Sabatier · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polypyrimidine tract-binding protein (PTB) is a splicing regulator that also plays a positive role in pre-mRNA 3' end processing when bound upstream of the polyadenylation signal (pA signal). Here, we address the mechanism of PTB stimulatory function in mRNA 3' end formation. We identify PTB as the protein factor whose binding to the human beta-globin (HBB) 3' UTR is abrogated by a 3' end processing-inactivating mutation. We show that PTB promotes both in vitro 3' end cleavage and polyadenylation and recruits directly the splicing factor hnRNP H to G-rich sequences associated with several pA signals. Increased binding of hnRNP H results in stimulation of polyadenylation through a direct interaction with poly(A) polymerase. Therefore, our results provide evidence of a concerted regulation of pA signal recognition by splicing factors bound to auxiliary polyadenylation sequence elements.

Indexed as

RNA 3' End Processing3' Untranslated RegionsBase Sequencebeta-GlobinsConserved SequenceHeterogeneous-Nuclear Ribonucleoprotein Group F-HHumansPoly APolyadenylationPolypyrimidine Tract-Binding ProteinRegulatory Sequences, Ribonucleic AcidRNA, MessengerRNA Precursors3' Untranslated Regionsbeta-GlobinsHeterogeneous-Nuclear Ribonucleoprotein Group F-HPoly APolypyrimidine Tract-Binding ProteinRegulatory Sequences, Ribonucleic AcidRNA, MessengerRNA Precursors

Identifiers

PMID19506027
PMCPMC2724285
OpenAlexW2166441406

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.